Ischaemic preconditioning improves upper-body endurance performance without altering V̇O2 kinetics.

PURPOSE: Whilst pre-exercise ischaemic preconditioning (IPC) can improve lower-body exercise performance, its impact on upper-limb performance has received little attention. This study examines the influence of IPC on upper-body exercise performance and oxygen uptake (V̇O2) kinetics. METHODS: Eleven recreationally-active males (24 ± 2 years) completed an arm-crank graded exercise test to exhaustion to determine the power outputs at the ventilatory thresholds (VT1 and VT2) and V̇O2peak (40.0 ± 7.4 ml·kg-1·min-1). Four main trials were conducted, two following IPC (4 × 5-min, 220 mmHg contralateral upper-limb occlusion), the other two following SHAM (4 × 5-min, 20 mmHg). The first two trials consisted of a 15-minute constant work rate and the last two time-to-exhaustion (TTE) arm-crank tests at the power equivalents of 95% VT1 (LOW) and VT2 (HIGH), respectively. Pulmonary V̇O2 kinetics, heart rate, blood-lactate concentration, and rating of perceived exertion were recorded throughout exercise. RESULTS: TTE during HIGH was longer following IPC than SHAM (459 ± 115 vs 395 ± 102 s, p = .004). Mean response time and change in V̇O2 between 2-min and end exercise (ΔV̇O2) were not different between IPC and SHAM for arm-cranking at both LOW (80.3 ± 19.0 vs 90.3 ± 23.5 s [p = .06], 457 ± 184 vs 443 ± 245 ml [p = .83]) and HIGH (96.6 ± 31.2 vs 92.1 ± 24.4 s [p = .65], 617 ± 321 vs 649 ± 230 ml [p = .74]). Heart rate, blood-lactate concentration, and rating of perceived exertion did not differ between conditions (all p ≥ .05). CONCLUSION: TTE was longer following IPC during upper-body exercise despite unchanged V̇O2 kinetics.HighlightsWhilst pre-exercise ischaemic preconditioning can improve lower-body exercise performance and alter V̇O2 kinetics, its impact on upper-limb performance has received little attention.An acute bout of ischaemic preconditioning prior to arm-crank ergometry exercise significantly improved time to exhaustion compared to a sham control condition.V̇O2 kinetics in response to ischaemic preconditioning remained unchanged, suggesting alternative mechanisms may explain performance improvements.

Differences in serum IL-6 response after 1 °C rise in core body temperature in individuals with spinal cord injury and cervical spinal cord injury during local heat stress.

OBJECTIVES: Passive rise in core body temperature achieved by head-out hot water immersion (HHWI) results in acute increases in serum interleukin (IL)-6 but no change in plasma adrenaline in patients with cervical spinal cord injury (CSCI). The purpose of the present study was to determine the mechanism of heat stress-induced increase in serum IL-6. SETTING: A cross-sectional study. METHODS: The study subjects were nine with CSCI, ten with thoracic and lumbar spinal cord injury (TLSCI) and eight able-bodied (AB) subjects. Time since injury was 16.1 ± 3.4 years in TLSCI and 16.4 ± 4.1 years in CSCI. Subjects were subjected to lower-body heat stress (LBH) by wearing a hot water-perfused suit until 1 °C increase in core temperature. The levels of serum IL-6, plasma adrenaline, tumour necrosis factor (TNF)-α, C-reactive protein (CRP), and counts of blood cells were measured at normothermia and after LBH. RESULTS: Serum IL-6 concentrations increased significantly immediately after LBH in all the three groups. ΔIL-6% was lower in CSCI subjects compared with AB subjects. Plasma adrenaline concentrations significantly increased after LBH in AB and TLSCI subjects, but did not change throughout the study in CSCI subjects. Cardiac output and heart rate increased at the end of LBH in all three groups. CONCLUSIONS: Under a similar increase in core temperature, ΔIL-6% was lower in the CSCI group compared with the AB group. These findings suggest that the observed rise in IL-6 during hyperthermia is mediated, at least in part, by plasma adrenaline.

Acute and chronic effects of hot water immersion on inflammation and metabolism in sedentary, overweight adults.

Regular exercise-induced acute inflammatory responses are suggested to improve the inflammatory profile and insulin sensitivity. As body temperature elevations partly mediate this response, passive heating might be a viable tool to improve the inflammatory profile. This study investigated the acute and chronic effects of hot water immersion on inflammatory and metabolic markers. Ten sedentary, overweight men [body mass index (BMI): 31.0 ± 4.2 kg/m2, mean ± SD] were immersed in water set at 39°C for 1 h (HWI) or rested for 1 h at ambient temperature (AMB). Venous blood was obtained before the session, immediately postsession, and 2 h postsession for assessment of monocyte intracellular heat shock protein-72 (iHsp72) and plasma concentrations of extracellular Hsp72 (eHsp72), interleukin-6 (IL-6), fasting glucose, insulin, and nitrite. Thereafter, participants underwent a 2-wk intervention period, consisting of 10 hot water immersion sessions (INT). Eight BMI-matched participants (BMI: 30.0 ± 2.5 kg/m2) were included as control (CON). Plasma IL-6 and nitrite concentrations were higher immediately following HWI compared with AMB (IL-6 P < 0.001, HWI: 1.37 ± 0.94 to 2.51 ± 1.49 pg/ml; nitrite P = 0.04, HWI: 271 ± 52 to 391 ± 72 nM), whereas iHsp72 expression was unchanged ( P = 0.57). In contrast to resting iHsp72 expression ( P = 0.59), fasting glucose ( P = 0.04; INT: 4.44 ± 0.93 to 3.98 ± 0.98 mmol/l), insulin ( P = 0.04; INT: 68.1 ± 44.6 to 55.0 ± 29.9 pmol/l), and eHsp72 ( P = 0.03; INT: 17 ± 41% reduction) concentrations were lowered after INT compared with CON. HWI induced an acute inflammatory response and increased nitric oxide bioavailability. The reductions in fasting glucose and insulin concentrations following the chronic intervention suggest that hot water immersion may serve as a tool to improve glucose metabolism. NEW & NOTEWORTHY A single hot water immersion (HWI) session induces an acute increase in plasma interleukin-6 and nitrite concentrations but does not acutely elevate heat shock protein-72 expression in monocytes [intracellular Hsp72 (iHsp72)]. A chronic HWI intervention reduces fasting glucose and insulin concentrations in the absence of changes in resting iHsp72. Therefore, HWI shows potential as a strategy to combat chronic low-grade inflammation and improve glucose metabolism in individuals without the physical capacity to do so using exercise.

The effect of passive heating on heat shock protein 70 and interleukin-6: A possible treatment tool for metabolic diseases?

Increasing physical activity remains the most widely publicized way of improving health and wellbeing. However, in populations that benefit most from exercise (EX), adherence is often poor and alternatives to EX are important to bring about health improvements. Recent work suggests a role for passive heating (PH) and heat shock proteins (HSP) in improving cardio-metabolic health. The aim of this study was to investigate the expression of HSP70 and interleukin-6 in response to either EX or PH and the subsequent effect on glucose control. Fourteen males volunteered and were categorized lean (BMI 23.5 ± 2.2 kg·m-2) or overweight (29.2 ± 2.7 kg·m-2) and completed 60 minutes of either moderate cycling at a fixed rate of metabolic heat production (EX) or warm water immersion in 40°C water (PH). Extracellular HSP70 increased from baseline in both conditions with no differences between PH (0.98 ± 1.1 ng·mL-1) or EX (0.84 ± 1.0 ng·mL-1, p = 0.814). IL-6 increased following both conditions with a two-fold increase after PH and four-fold after EX. Energy expenditure increased by 61.0 ± 14.4 kcal·h-1 (79%) after PH. Peak glucose concentration after a meal immediately following PH was reduced when compared with EX (6.3 ± 1.4 mmol·L-1 versus 6.8 ± 1.2 mmol·L-1; p < 0.05). There was no difference in 24-hour glucose area under the curve (AUC) between conditions. These data indicate the potential for thermal therapy as an alternative treatment and management strategy for those at risk of developing metabolic disease where adherence, or ability to EX, may be compromised.

Hot water immersion induces an acute cytokine response in cervical spinal cord injury.

PURPOSE: The dysfunctional sympathetic nervous system in individuals with cervical spinal cord injury (CSCI) impairs adrenergic responses and may, therefore, contribute to the blunted post-exercise cytokine response. The purpose of this study was to investigate an alternative way to exercise to induce an acute cytokine response by passive core temperature elevation in CSCI. METHODS: Seven male participants with a motor complete CSCI and 8 male able-bodied controls were immersed for 60 min in water set at a temperature 2 °C above the individuals' resting oesophageal temperature. Blood was collected pre, post, and every hour up to 4 h post-immersion. RESULTS: Hot water immersion resulted in an IL-6 plasma concentration mean increase of 133 ± 144 % in both groups (P = 0.001). On a group level, IL-6 plasma concentrations were 68 ± 38 % higher in CSCI (P = 0.06). In both groups, IL-8 increased by 14 ± 11 % (P = 0.02) and IL-1ra by 18 ± 17 % (P = 0.05). Catecholamine plasma concentrations were significantly reduced in CSCI (P < 0.05) and did not increase following immersion. CONCLUSIONS: Passive elevation of core temperature acutely elevates IL-6, IL-8 and IL-1ra in CSCI despite a blunted adrenergic response, which is in contrast to earlier exercise interventions in CSCI. The present study lays the foundation for future studies to explore water immersion as an alternative to exercise to induce an acute cytokine response in CSCI.

Blood lactate and ventilatory thresholds in wheelchair athletes with tetraplegia and paraplegia.

PURPOSE: The purpose of this study was to analyse the influence of spinal cord injury level on blood lactate (BLa) and ventilatory thresholds. METHODS: Ten athletes with tetraplegia (TETRA) and nine athletes with paraplegia (PARA) performed a graded wheelchair propulsion treadmill exercise step test to exhaustion. The aerobic and anaerobic BLa thresholds, the ventilatory threshold and the respiratory compensation point (RCP) were determined. RESULTS: The BLa thresholds were determined in 34 of 38 cases, ventilatory thresholds and RCPs in 31 of 38 cases. The anaerobic BLa threshold (76 ± 7 % [Formula: see text]) and the RCP (77 ± 8 % [Formula: see text]) did not differ significantly from each other (P = 0.92), with a coefficient of variation of 4.8 ± 3.4 % between thresholds. All other thresholds differed significantly from each other (P < 0.05). Thresholds expressed as the percentage of peak oxygen uptake did not differ between TETRA and PARA (P > 0.05) despite altered breathing in TETRA, which included a higher ventilatory equivalent for oxygen and a lower tidal volume. CONCLUSION: Measuring BLa leads to a higher threshold determination rate compared with ventilatory data and the anaerobic BLa threshold can be used to predict the RCP. The altered breathing in TETRA does not seem to have a pronounced effect on the ventilatory threshold or the RCP.

Spinal cord injury: known and possible influences on the immune response to exercise.

A spinal cord injury (SCI) can increase the risk of infection by impacting on many aspects of immune function; one particularly well-documented observation is a reduction in lymphocyte numbers. The vast majority of lymphoid cells express adrenergic receptors. Therefore, autonomic function loss and concomitant alterations in resting and post-exercise catecholamine concentrations, particularly so in individuals with a tetraplegia, may impact directly on immune cells and depress immunity. Other factors are further likely to contribute, examples including altered muscular, endocrine and cardiovascular function following SCI. However, some alterations, such as increases in natural killer cell cytotoxicity following exercise in those with a tetraplegia, are unrelated to the catecholamine response. Likewise, mucosal immunity in individuals with a tetraplegia appears to be similarly influenced by exercise as in the able-bodied population. Indeed, rehabilitation therapy and exercise can increase some measures of immunity and autonomic function in those with an SCI. It is therefore possible that compensatory mechanisms offset disability-related detriments. This may be by way of sympathetic reflex activity, receptor hypersensitivity, or parasympathetic and neuroendocrine adjustments. Future work needs to explore these mechanisms further to clarify the implications of an SCI on the immune response to exercise and susceptibility to infection. In this article, we review the impacts of an SCI on immune, and specifically, exercise immune function. The relevant anatomical and physiological foundations of the immune system are first briefly laid out in order to understand the potential impacts of neural and neuroendocrine dysfunction on the immune system. With the limited number of human studies available, we have then aimed specifically to gather all relevant existing literature on exercise immunology in individuals with an SCI in patient, recreationally active and athlete populations. We believe that an understanding of the impacts of exercise can provide a tool to help maintain or improve health in individuals with an SCI. A comprehensive literature search was conducted using the search engines PubMed, SPORTDiscus, Web of Science and Zetoc, search period June 2012-February 2013. Key words employed included spinal cord injury, immunology, exercise, paraplegic, tetraplegic, upper body exercise, interleukin, immunoglobulin, sympathetic, and parasympathetic. All articles and articles derived from their reference lists were checked for their suitability.

Mucosal immune responses during court training in elite tetraplegic athletes.

STUDY DESIGN: Experimental study. OBJECTIVES: To examine salivary secretory immunoglobulin A (sIgA) responses and α-amylase activity during court training in highly trained tetraplegic athletes. SETTING: Loughborough, UK. METHODS: Seven highly trained wheelchair rugby athletes with tetraplegia performed two separate wheelchair rugby court training sessions, lasting 23 and 41.5 min, respectively, with either an aerobic or an interval focus. Timed, unstimulated saliva samples were obtained pre, post and 30 min post exercise and analysed for sIgA and α-amylase. Furthermore, blood lactate concentration and rating of perceived exertion (RPE) immediately after training were measured. RESULTS: sIgA secretion rate and α-amylase were unaffected by exercise during both sessions. However, the increases of sIgA concentration (30 min post exercise: +67 ± 29%) during the aerobic session were accompanied by decreases in saliva flow rate (-35 ± 22%). Athletes' physiological responses to exercise document the highly strenuous nature of the sessions, with blood lactate concentrations reaching 8.1 ± 1.0 and 8.7 ± 1.6 mmol l(-1) and RPE reaching 18(17,18) and 16(15,17) for the aerobic and the interval session, respectively. CONCLUSION: Acute bouts of highly strenuous exercise do not have negative impacts on the mucosal immune response in tetraplegic athletes, nor do they influence the production of α-amylase, a marker of sympathetic nervous activity. This contrasts responses previously observed in able-bodied athletes. The disruption of the sympathetic nervous system may prevent the downregulation of sIgA secretion rate following intense exercise, which is a response previously observed in able-bodied athletes.

Submaximal exercise responses in tetraplegic, paraplegic and non spinal cord injured elite wheelchair athletes.

It remains unclear whether similar exercise prescription, based on physiological markers, can be applied to subgroups of wheelchair athletes with different disabilities. Therefore, 25 wheelchair athletes, divided into three subgroups [eight tetraplegic (TETRA), nine paraplegic (PARA) and eight non spinal cord injured (NON-SCI)], performed an exercise test consisting of incremental submaximal stages, covering a range from 40% to 80% peak oxygen uptake (%VO(2peak) ). Oxygen uptake (VO(2)), heart rate (HR), blood lactate concentration (BLa) and rating of perceived exertion (RPE) were obtained for each stage. Expressed as a function of BLa, no differences were found between subgroups with respect to %VO(2peak) (group mean ± SD: 1.0 mmol/L: 53.9 ± 9.9%; 2.0 mmol/L: 70.7 ± 7.5%; 3.0 mmol/L: 78.5 ± 7.7%) and RPE [group mean (lower and upper quartile): 1.0 mmol/L: 10.8 (9.9, 12.2); 2.0 mmol/L: 13.6 (12.7, 14.3); 3.0 mmol/L: 14.9 (13.7, 16.5)]. Furthermore, no differences were found in the coefficient of determination (R(2) ) of the HR-VO(2) relationship in any of the subgroups (TETRA: 0.90 ± 0.12; PARA: 0.97 ± 0.02; NON-SCI: 0.96 ± 0.04). These results suggest that exercise prescription using measurements of VO(2), BLa or RPE can be based on the same recommendations in all the subgroups studied. This finding has added value for TETRA athletes, as it offers alternatives to HR monitoring.

Continuous spinal anesthesia for cesarean section in a parturient with severe recurrent peripartum cardiomyopathy.

The anesthetic management of labor and delivery in patients with peripartum cardiomyopathy is not well defined. Using continuous spinal anesthesia in such a rare clinical situation has not been previously reported. A patient with recurrent peripartum cardiomyopathy presented in congestive heart failure for emergent cesarean section. Continuous spinal anesthesia was successfully employed as the anesthetic technique for the procedure. In addition, it also markedly reduced the patient's symptoms. Continuous spinal anesthesia is a reliable, rapidly titratable technique, which provides excellent analgesia with minimal undesirable hemodynamic changes for patients with peripartum cardiomyopathy undergoing cesarean delivery.

Combined spinal and epidural anesthesia for labor and cesarean delivery in a patient with Guillain-Barre syndrome.

BACKGROUND AND OBJECTIVES: The anesthetic management of labor, delivery, and cesarean delivery in patients with active or resolving Guillain-Barre syndrome is not well defined. Using a combined spinal and epidural (CSE) technique in such a rare clinical situation has not been previously reported. CASE REPORT: A 32-year-old woman gravida 2, para 0 was diagnosed with Guillain-Barre syndrome at 21 weeks of pregnancy. Paralysis spread up to the T4 level. Three months later, she was admitted for labor at term. She presented in severe labor pain and it was decided to proceed with CSE analgesia. No unusual hemodynamic instability, signs of autonomic dysfunction, or increased sensitivity to local anesthetics was noted. After several hours, delivery by cesarean section was required and epidural anesthesia was then used. The patient had an uncomplicated postpartum course. CONCLUSION: Careful evaluation and documentation of the patient's baseline neurological status, a thorough discussion with the patient regarding the risks and benefits of the technique for labor analgesia, and an appreciation of the limited experience with this kind of clinical situation are important.

Peptide immunization indicates that CD8+ T cells are the dominant effector cells in trinitrophenyl-specific contact hypersensitivity.

The identity of the effector T cell population involved in contact hypersensitivity is still questionable with evidence promoting both CD4+ or CD8+ T cells. Previous experimental studies have relied on the in vivo depletion of T cell subsets using antibody, or the use of knock-out mice with deficiencies in either CD4+ or CD8+ T cell-mediated immunity. To address the role of the class I- and class II-mediated pathways of T cell activation in contact hypersensitivity responses in mice with an intact immune system, we utilized various trinitrophenyl-derivatized peptides, which bind specifically with H-2Kb (major histocompatibility complex class I) or H-2I-Ab (major histocompatibility complex class II). The subcutaneous injection of major histocompatibility complex class II-specific, but not of class I-binding, hapten-derivatized peptides in incomplete Freund's adjuvant induced specific, albeit low, contact hypersensitivity responsiveness to trinitrochlorobenzene. When bone-marrow-derived dendritic cells, however, were pulsed with the same peptides and administered intradermally, the opposite result was observed, namely that the class I binding peptides induced contact hypersensitivity responses similar to that observed after epicutaneous trinitrochlorobenzene application. In contrast, dendritic cells pulsed with major histocompatibility complex class II binding peptides did not reproducibly sensitize for contact hypersensitivity responses. Surprisingly, both immunization protocols efficiently induced CD8+ effector T cells. These results support the notion that CD8+ T cells are the dominant effector population mediating contact hypersensitivity responsiveness and that the CD4+ T cell subset only contributes little if at all.

Regional anesthesia and local anesthetic-induced systemic toxicity: seizure frequency and accompanying cardiovascular changes.

We sought to determine the contemporary frequency of seizures, and the associated cardiovascular changes, resulting from local anesthetic-induced seizures in all patients undergoing brachial plexus, epidural, and caudal regional anesthetics. We investigated the following variables: development and treatment of seizure or cardiac arrest during the regional anesthetic, type of anesthetic (including local anesthetic used), gender, age, ASA physical status class and type of operation (elective or emergent). In addition, each patient who experienced a seizure underwent retrospective review of the acute event to determine the arterial blood pressure and heart rate changes accompanying the seizure, as well as details of the regional block technique. There was a significant difference between the rate of seizure development between epidural, brachia, and caudal anesthetics, with caudal > brachial > epidural. A significant difference was also noted in the rate of seizure development within types of brachial block, with supraclavicular and interscalene > axillary. No adverse cardiovascular, pulmonary or nervous system events were associated with any of the seizures, including the 16 patients who received bupivacaine blocks. The frequency of local anesthetic-induced seizures stratified by block type has a wide range, and cardiovascular collapse after bupivacaine-associated seizure has a low incidence.

Fetal heart rate variability and cerebral oxygen consumption in fetal sheep during asphyxia.

This study was designed to examine the relationship between fetal heart rate variability and fetal cerebral oxygen uptake. Fetal sheep were chronically prepared with catheters and electrodes to determine cerebral blood flow (microsphere method), cerebral arteriovenous oxygen difference, and the electrocardiogram. An adjustable occluder was placed on the maternal common internal iliac artery to induce fetal asphyxia by reducing uterine blood flow. Fetal heart rate variability tended to decrease in the first 11 min of asphyxia, when cerebral oxygen consumption was approximately 53% of control. Despite stable cerebral oxygen consumption and worsening metabolic acidosis, however, fetal heart rate variability progressively returned towards normal by 36 min. There was no relationship between the depression of FHR variability and the degree of reduction of cerebral oxygen consumption. Nor was there any relationship between an alteration in regional cerebral blood flow or myocardial blood flow and the return of FHR variability with increasing duration of asphyxia. We conclude that there is an association between loss of fetal heart rate variability and reduced cerebral oxygen consumption, but the reduced variability does not persist with time at this degree of reduced cerebral metabolism in fetal sheep. This appears to be at variance with human clinical experience. Among the explanations for this may be insufficiently severe asphyxia, a species difference, removal of an inhibitor to FHR variability, or progressive use of other substrates for metabolism.